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American Journal of Epidemiology Advance Access originally published online on November 17, 2007
American Journal of Epidemiology 2008 167(2):169-177; doi:10.1093/aje/kwm291
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American Journal of Epidemiology © The Author 2007. Published by the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

ORIGINAL CONTRIBUTIONS

Variations in Prenatal Sociodemographic Factors associated with Intellectual Disability: A Study of the 20-Year Interval between Two Birth Cohorts in Northern Finland

Ulla Heikura1, Anja Taanila1, Anna-Liisa Hartikainen2, Päivi Olsen3, Sirkka-Liisa Linna4, Lennart von Wendt5 and Marjo-Riitta Järvelin1,6

1 Department of Public Health Science and General Practice, Faculty of Medicine, University of Oulu, Oulu, Finland
2 Department of Obstetrics and Gynecology, University Hospital of Oulu, Oulu, Finland
3 Department of Child Neurology, University Hospital of Oulu, Oulu, Finland
4 Clinic of Child Psychiatry, University Hospital of Oulu, Oulu, Finland
5 Hospital for Children and Adolescents, University Hospital of Helsinki, Helsinki, Finland
6 Department of Epidemiology and Public Health, School of Medicine, Imperial College London, London, United Kingdom

Correspondence to Dr. Marjo-Riitta Järvelin, Department of Epidemiology and Public Health, School of Medicine, Imperial College London, Norfolk Place, London W2 1PG, United Kingdom (e-mail: m.jarvelin{at}ic.ac.uk).

Received for publication October 23, 2006. Accepted for publication September 11, 2007.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
The authors followed two cohorts of children born in northern Finland in 1966 (n = 12,058) and 1985–1986 (n = 9,432) to examine whether associations between maternal sociodemographic factors assessed during pregnancy and intellectual disability in the offspring changed over a 20-year interval. Both of the cohorts were followed up to the age of 11.5 years using similar methods and definitions of intellectual disability. Data on sociodemographic factors were based on comparable questionnaires returned by the mothers during the 25th week of gestation. Despite an interval of 20 years between the cohorts, the main indicators of socioeconomic disadvantage and maternal multiparity remained as having the largest impact on the incidence of intellectual disability, while single factors such as older maternal age at delivery, being single, and living in a remote area lost their association with intellectual disability. Over 20 years, prepregnancy maternal obesity (body mass index ≥30) became a newly associated factor (adjusted odds ratio = 2.8, 95% confidence interval: 1.5, 5.3). A future challenge is to explore the mediating mechanisms between intellectual disability and its associated preventable intergenerational environmental or lifestyle factors.

cohort studies; demography; family characteristics; mental retardation; pregnancy; prenatal exposure delayed effects; social class

Abbreviations: CI, confidence interval; ID, intellectual disability; IQ, intelligence quotient; NFBC, Northern Finland Birth Cohort; OR, odds ratio


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
The etiology of intellectual disability (ID), defined as an intelligence quotient (IQ) of 70 or lower, can be viewed over generations and the individual's own life course as a multifactorial construct of four interacting categories of risk factors: biomedical, social, behavioral, and educational (1). The traditional classification of ID etiology is based on the timing and mechanism of damage to the central nervous system (2). Prenatal (from fertilization to birth) risk of ID has been linked to genetic and other biomedical factors, poverty, maternal malnutrition, and a lack of access to prenatal care (social factors); to maternal smoking, substance use, and alcohol use during pregnancy (behavioral factors); and to parental cognitive disability with a lack of readiness for parenthood (educational factors). Correspondingly, paranatal risk factors consist of diseases incurred within 1 week before birth (e.g., herpesvirus infection), complications arising at birth, and neonatal disorders, as well as poor access to delivery services, parental rejection of caretaking, lack of emotional or practical support, and insufficient or limited referral for medical intervention services up to 4 weeks of age. Postnatal etiology includes cases in which the timing of the central nervous system damage occurs after 4 weeks of life (i.e., after the neonatal period), up to age 18 years (1).

Studies on sociodemographic risk factors for ID have suggested that older age, low maternal educational level, and high birth order of the child are associated with increased risk of ID (3–5). In addition, lower socioeconomic status is especially overrepresented among families that have a child with mild ID (IQ 50–70) (6–10). Although a single adverse social marker does not necessarily lead to ID, the simultaneous presence of several negative factors may lead to an increased risk of developmental disabilities (11). The challenge is to identify changes in and the relative importance of preventable environmental or lifestyle factors/effects that can be passed down through a family and may have an adverse influence on the development of intellectual capacity in the offspring.

The current study was based on two large population-based birth cohorts with similar overall incidences of ID (12.6/1,000 livebirths) (12): the Northern Finland Birth Cohort of 1966 (NFBC 1966) and the Northern Finland Birth Cohort of 1985–1986 (NFBC 1986). In NFBC 1966, the etiology of ID was prenatal in 56 percent of cases (59 percent in NFBC 1986), paranatal in 17 percent (3 percent in NFBC 1986), postnatal in 3 percent (4 percent in NFBC 1986), and unclassified in 24 percent (34 percent in NFBC 1986) (13). In the present study, we investigated maternal sociodemographic factors assessed during pregnancy that were potentially associated with ID in the offspring and explored their relative importance in and impact on ID risk within and between these cohorts.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 References
 
Study populations and methods
Two genetically homogenous cohorts of Caucasian children born 20 years apart in the two northernmost provinces of Finland, Oulu and Lapland, were studied. The mothers were enrolled during routine visits to communal maternity health centers during the 25th week of gestation. These visits were/are free of charge, with a participation rate of nearly 100 percent. The first cohort, NFBC 1966, was based on 12,058 liveborn children (pregnancy continued for at least 28 weeks; coverage, 96 percent of those eligible) with expected dates of birth in the year 1966 (14). The second, NFBC 1986, was based on 9,432 liveborn children (pregnancy continued for ≥24 weeks; 99 percent of those eligible) with expected dates of birth between July 1, 1985, and June 30, 1986 (15).

Data on the cohorts were collected from multiple interchangeable sources. No separate examinations were conducted for either cohort; we relied on existing clinical practice and the referral system. For both cohorts, data on ID were based on standardized psychometric tests administered by a psychologist. The test scores were collected from hospitals, institutions for children with ID, family counseling centers, and school psychologists. Psychometric assessment of the level of the child's ID was available for 71.5 percent of children with ID in NFBC 1966 and 81.5 percent of children with ID in NFBC 1986. If there was no such assessment but it was evident that the child had ID based on the diagnosis of a disorder/disease, then we classified the child's level of ID on a clinical basis. The process and the identification of children with ID included tracing the children who had moved away from northern Finland (12).

For NFBC 1966, follow-up of the children was originally conducted by Rantakallio and von Wendt (16), who collected follow-up data on ID at various ages until the children were 14 years old in 1980. At the time of their data collection in 1980/1981, 17 percent of the cohort children were living in other parts of Finland or had emigrated to other countries. All but 14 of the children who had moved away from the study area were traced in 1980/1981 (16). For NFBC 1986, collection of data on ID was carried out between 1985 and 2000. In 1998, 8.0 percent of the children were living in other parts of Finland or living abroad; for those children, data on ID were collected from the same sources as for children living within the study area, with the exception that for the latter group the information was only available until the time of emigration. In both cohorts, the data were collected until the children reached the age of 11.5 years (up to June 30, 1977).

Definitions
In both cohorts, we followed children up to the age of 11.5 years. Similar study designs, data ascertainment methods, and definitions of ID were used. The definition of ID as an IQ of 70 or below followed the Finnish version of the International Classification of Diseases, Ninth Revision (17). Severe ID was defined as an IQ below 50 and mild ID as an IQ of 50–70, based on an individually administered standardized psychometric test or a clinical developmental assessment. The incidence of ID was defined as the number of new cases arising from birth to the end of the follow-up time (11.5 years), per 1,000 livebirths. The incidence of severe ID was 7.6/1,000 in NFBC 1966 and 5.1/1,000 in NFBC 1986, and the incidence of mild ID was 5.0/1,000 in NFBC 1966 and 7.5/1,000 in NFBC 1986 (12).

Data on sociodemographic factors in both cohorts were based on questionnaires with similar and comparable core questions administered upon enrollment at the maternity health centers. Socioeconomic status was assessed in four classes according to occupation and its prestige (18). Socioeconomic status was assessed separately for the mother and father; the socioeconomic status of the family was determined by the father's socioeconomic status or, when this information was missing, by the mother's. Maternal education was defined as compulsory basic education or more than compulsory education. Since the mothers' data were collected during actual pregnancy, a nulliparous woman (parity of 0) was defined as a woman who had had no previous deliveries and a multiparous woman was defined as a woman with four or more previous deliveries; the reference category was 1–3 previous deliveries. Prepregnancy weight (kg) was reported by the mothers, and height (cm) was measured at the maternity health-care center or self-reported (19). Prepregnancy body mass index (weight (kg)/height (m)2) was divided into four categories: 1) thin (<20.0), 2) normal (20.0–24.9), 3) overweight (25.0–29.9), and 4) obese (≥30.0).

Analytic strategy and statistical analysis
We made a systematic analytic plan for the data exploration, and final analyses were based on the literature and the availability of data. In the initial stage, we conducted univariate association analyses between potential contributory factors and ID utilizing extensive data collected over the years. From these analyses, the factors of main importance were forwarded into further analyses. In the final stage, we firstly estimated the unadjusted incidence of ID per 1,000 livebirths and odds ratios for the categories of each potential risk factor (selected from a vast amount of data, as indicated above) separately for both cohorts. Secondly, we conducted a Breslow-Day test for homogeneity of the risk of ID (odds ratios) between NFBC 1966 and NFBC 1986 according to each factor to estimate changes in the risk indicators between the cohorts (20). Thirdly, the most relevant risk factors for ID were considered for multivariate logistic regression analyses, based on careful review of the database and significance/relative importance in exploratory analyses and the literature. Fourthly, we separately calculated population attributable risks using the most important explanatory factors for ID for NFBC 1966 and NFBC 1986 (21, 22). The population attributable risk takes into account both individual-level risk and the prevalence of a given risk factor in the population. Even if a causal relation cannot be established, the population attributable risk will still identify the group that has the largest impact on the overall rate or number of cases in the population. This high-risk group can be targeted for services or programs (4).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 References
 
Table 1 shows sociodemographic characteristics and the risk of ID according to the sociodemographic factors in and between NFBC 1966 and NFBC 1986. Comparison of the maternal and familial sociodemographic factors between the cohorts shows that there were favorable changes in the age distribution; for example, the proportions of young and old mothers diminished, as did the percentage of multiparous women, by one half over the 20-year period. The proportion of lean mothers (body mass index <20) doubled, but that of obese mothers (body mass index ≥30) remained unaltered (3.8 percent). The mothers in NFBC 1986 made better use of maternity services. The proportion of rare visitors (six visits or less) at the maternity health centers was 4.7 times higher in NFBC 1966. Educational level improved, and the proportion of higher socioeconomic status women (professional and skilled workers) increased from one third to two thirds. In NFBC 1966, 41 percent of the mothers lived in remote areas, as compared with 21 percent in NFBC 1986.


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  		TABLE 1. Distribution of children and incidence of intellectual disability in the Northern Finland Birth Cohort, according to sociodemographic factors, 1966 and 1986

 
In NFBC 1966, mothers who were older, were multiparous, were unmarried, used maternity health-care services rarely, had only compulsory education, were farmers or unskilled workers, or lived in remote areas had an increased risk of having a child with ID. In NFBC 1986, the corresponding associated factors were maternal multiparity, maternal obesity (body mass index ≥30), a low level of education, and being a farmer or an unskilled worker (table 1).

The test for homogeneity of the unadjusted odds ratios between the cohorts showed that there were no other statistically significant changes over time in sociodemographic factors associated with total ID, except for maternal obesity (p = 0.05) (table 1). When results were evaluated by severity of ID, the unadjusted odds ratios (data not shown) indicated that for severe ID, older maternal age at the time of delivery (p = 0.01) and living in a remote area (p = 0.056) lost their effects as major unfavorable associated factors over the 20-year period. For mild ID, obesity (p = 0.03) and multiparity (p = 0.05) appeared as newly associated unfavorable factors in NFBC 1986.

Multivariate logistic regression models were fitted for all children with ID and separately for children with severe and mild ID. The maternal covariates chosen were age, parity, body mass index, marital status, socioeconomic status, and place of residence, because of their strong univariate associations with ID. In NFBC 1966, older maternal age (odds ratio (OR) = 1.8, 95 percent confidence interval (CI): 1.1, 2.9), multiparity (OR = 1.7, 95 percent CI: 1.0, 2.8), and being unmarried (OR = 2.3, 95 percent CI: 1.0, 5.0) were independently associated with total ID, whereas in NFBC 1986, those factors were multiparity (OR = 2.0, 95 percent CI: 1.2, 3.6), obesity (OR = 2.8, 95 percent CI: 1.5, 5.3), low socioeconomic status (being an unskilled worker: OR = 2.5, 95 percent CI: 1.6, 4.0), and being a farmer (OR = 2.6, 95 percent CI: 1.1, 6.1).

Table 2 shows results from the adjusted multivariate analyses of the factors associated with level of ID. The results indicate that in NFBC 1966, older maternal age, multiparity, being unmarried, and living in a remote area were independently associated with severe ID. Correspondingly, in NFBC 1986, those factors were low socioeconomic status (being an unskilled worker) and nulliparity. With regard to mild ID in 1966, low maternal body mass index and being a farmer appeared as associated factors, while in 1986 those factors were obesity, multiparity, and being a farmer or unskilled worker.


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  		TABLE 2. Unadjusted and adjusted odds ratios (multiple logistic regression) for severe and mild intellectual disability in the Northern Finland Birth Cohort, 1966 and 1986

 
We conducted further analyses to study the interactions of maternal body mass index and parity, that is, the possible additive effects (figures 1 and 2). In NFBC 1966, a trend of increased risk of ID with increasing parity was detected only in the lowest maternal body mass index group (<20). The incidence of ID in the group with multiparity (≥3) and low body mass index was 2.9-fold higher than the overall incidence of ID in the whole population (36/1,000 vs. 12.6/1,000) (figure 1). In NFBC 1986, the incidence of ID was elevated in all parity categories for the obese mothers, showing a linear increase from 1.4-fold in nulliparae to 3.4-fold in multiparae in comparison with the overall incidence (12.6/1,000) (figure 2).


Figure 1
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  		FIGURE 1. Effect of the interaction between maternal parity and body mass index on risk of intellectual disability in the offspring, Northern Finland Birth Cohort, 1966.

 

Figure 2
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  		FIGURE 2. Effect of the interaction between maternal parity and body mass index on risk of intellectual disability in the offspring, Northern Finland Birth Cohort, 1986.

 
The highest population attributable risks for ID in order of single factors are seen in table 3. The factors indicating a low level of maternal education (compulsory education only, being an unskilled worker) and multiparity showed the highest attributable risks for ID in both cohorts. In NFBC 1966, 18.4 percent of ID was attributable to living in a remote area, whereas in NFBC 1986 it had nearly lost its impact for ID (1.9 percent). Having few contacts with antenatal care facilities accounted for only 3.1 percent of total ID in NFBC 1986, as compared with 13.6 percent in NFBC 1966.


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  		TABLE 3. Maternal sociodemographic factors associated with ≥5% population attributable risks of intellectual disability in the Northern Finland Birth Cohort, 1966 and 1986

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
References
 
Our study showed that over an interval of 20 years, indicators of socioeconomic disadvantage (a low level of education and low socioeconomic status) and multiparity had the largest impact on the incidence of ID in offspring. Only one new unfavorable sociodemographic factor associated with ID, namely maternal obesity, appeared. Being a single mother, living in a remote area, and being older at delivery lost their impact on offspring's risk of ID over time.

Variations in study design, the ID assessment criteria used, and methods applied for the identification of cases, as well as temporal and regional differences in maternity and social care, make direct comparisons of the sociodemographic factors associated with ID in different studies difficult. Thus, only tentative judgments can be made. Our study, which contained repeatedly collected data on two general population-based cohorts born 20 years apart in the same geographic areas with similar data collection methods and ID definitions, provided information about the changes occurring over time in sociodemographic factors associated with ID. This information is valuable in evaluating ID prevention efforts and general developments in health care (23).

The distribution of social class and family status indicators can vary remarkably from one country to another; this affects the contribution of these factors to ID. For instance, in our study, only about 11 percent of total ID was attributable to socioeconomic status in NFBC 1986, while in their cross-sectional US study, Camp et al. (4) found that the population attributable risk for low familial socioeconomic status was 50 percent among Black children with ID and 44 percent among Caucasian children with ID. It has, however, been a common general observation that children from lower socioeconomic classes have more health problems than children from higher socioeconomic classes (24). In our study, socioeconomic disadvantage was associated with both severe and mild ID in NFBC 1986, while in other studies low socioeconomic status was associated with mild ID only (6–10). The mediating factors between low familial socioeconomic status and poorer early cognitive function may include poor living conditions, impairment of children's physical health at birth, and inadequate provision of intellectual stimulation in the home environment (11, 25–27).

Our finding that the educational status distribution among mothers of children with severe ID (data not shown) was equal to the distribution in the background population (i.e., all mothers in NFBC 1986) and that a low level of maternal education was statistically significantly associated with mild ID only is consistent with the study by Drews et al. (5). Low maternal education may operate during pregnancy in such a way that these mothers may not be aware of the risk factors that can cause poor developmental outcomes in their children (3). During the child's early developmental years, maternal education may be related, among many other child-rearing factors, to knowledge of and access to early intervention services for children born at risk (25). A bioecologic approach emphasizes that the child and the family are elements of a larger developmental system in which multiple factors—such as the child's genotype, health, and the familial environment—interact. Interactive experiences between the child and his/her caregivers occur in the so-called zone of proximal development, in which maximal cognitive development is more likely to take place in an advantaged environment than in a disadvantaged one (28). Although the heritability of low intelligence has been estimated at 50 percent (29), geneticists have emphasized that it should not be considered a fixed level that is invariant over time and in differing social conditions; for example, a powerful environmental factor can change the impact of genetic factors accounting for the liability to show a particular trait in a population. A bioecologic model presumes that the contribution of heritability of intelligence decreases proportionally in the presence of social disadvantage, but results obtained in the few studies testing this hypothesis have been contradictory (30). Our study indicates how complex the associations are just between social factors and the intellectual level of the offspring, challenging investigators in future genetic studies to take into account multiple determinants of ID.

Overall maternal obesity in the study area had not increased in the 20 years leading up to 1986. Interestingly, among multiparae, leanness in NFBC 1966 and obesity in NFBC 1986 were associated with elevated risk of ID among offspring. This suggests that a weight difference in either direction from the optimal weight can be disadvantageous for risk of ID (31). To our knowledge, this is the first study in which the association of mothers' prepregnancy weight with ID in the offspring has been evaluated. A small-scale study on the association between maternal prepregnancy body mass index and general IQ at the average age of 5.3 years among 355 low-income African-American children was recently conducted in the United States (31). The findings of that study support our observation in that, after adjustment for other maternal covariates (age, receptive language ability, zinc supplementation status, smoking, alcohol use, the child's birth weight, child-care status, and home environment), the children with obese mothers (body mass index >29) had significantly lower general cognitive ability and nonverbal scores than did the children with normal-weight mothers (a mean general intellectual ability score of 80.0 vs. 84.5) (31).

There is a vast amount of data showing that disturbed intrauterine growth can affect fetal organ development and function. However, the mechanisms that might explain these associations are unclear. It is well known that overweight and obese women are at increased risk for various complications during pregnancy (preeclampsia, eclampsia, metabolic disturbances, infections) and at delivery, including increased risk of cesarean section, fetal and postnatal asphyxia, and offspring death (32, 33). These complications alone may lead to developmental disorders. The study by Watkins et al. (34) confirmed the previously established association between spina bifida and prepregnancy obesity and found an association for omphalocele, heart defects, and multiple anomalies among infants of obese women. One explanation for the adverse outcomes might be that obese women have metabolic alterations, such as hyperglycemia, elevated insulin or estrogen levels, or disturbed glucocorticoid metabolism, that increase risk for developmental disorders, including neurocognitive deficits (35). Obese women might also have nutritional deficits resulting from dieting behaviors or poor-quality diets that increase the risk of congenital anomalies. However, clear demonstration of causal effects of early nutrition on long-term neurodevelopment requires an experimental approach, which is not easily accomplished with pregnant women (31).

In conclusion, although the incidence of ID remained the same over a 20-year interval in northern Finland (12), changes in associated sociodemographic factors took place. Sociodemographic factors associated with ID risk in 1966, such as older maternal age, being single, and living in a remote area, lost their significance. This indicates that the associations between ID and maternal/familial sociodemographic factors are more wide-ranging than previously suggested. Temporal variations in these associations reflect changes in the living circumstances of the population. In our opinion, a rise in living standards and maternal educational levels, as well as improvements in the availability of high-quality antenatal and obstetric care (36) and health-care and social services (37), have at least partly contributed to these changes. Maternal obesity has appeared as a new disadvantageous factor associated with ID, while low socioeconomic status has remained as the major factor associated with ID. The next challenge is to uncover the mediating mechanism(s) between ID in the offspring and the associated environmental or lifestyle factors, such as maternal prepregnancy obesity.


   ACKNOWLEDGMENTS
 
This study was supported by the Rinnekoti Research Foundation (Espoo, Finland), the Alma and K. A. Snellman Foundation (Oulu, Finland), and the Academy of Finland (Helsinki, Finland).

Conflict of interest: none declared.


   References
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

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